Social reward: basic mechanisms and autism pathogenesis (#34)

Background: Social behaviors in species as diverse as
honey bees and humans promote group survival but often come at some cost to the
individual. Although reinforcement of
adaptive social interactions is ostensibly required for the evolutionary persistence
of these behaviors, the neural mechanisms by which social reward is encoded by
the brain are largely unknown.

Results: In mice oxytocin (OT) acts as a social
reinforcement signal within the nucleus accumbens (NAc) core, where it elicits
a presynaptically expressed long-term depression of excitatory synaptic
transmission in medium spiny neurons.
Although the NAc receives OT receptor-containing inputs from several
brain regions, genetic deletion of these receptors specifically from dorsal
raphe nucleus, which provides serotonergic (5-HT) innervation to the NAc,
abolishes the reinforcing properties of social interaction. Furthermore,
OT-induced synaptic plasticity requires activation of NAc 5-HT1b receptors, the
blockade of which prevents social reward.

Conclusions: These results demonstrate that the rewarding
properties of social interaction in mice require the coordinated activity of OT
and 5-HT in the NAc, a mechanistic insight with implications for understanding
the pathogenesis of social dysfunction in neuropsychiatric disorders such as
autism.